Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

316 Pharmacology > Exam 2: Thrombocytes, Hemostasis, and Alterations in function > Flashcards

Exam 2: Thrombocytes, Hemostasis, and Alterations in function Flashcards

1
Q

Thrombocytes

A

Platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Thrombopoiesis

A

Stimulated by thrombopoitein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Thrombopoietin is a

A

Hormone growth factor produced by liver, kidney, bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Do thrombocytes have a nuclei?

A

No! they do not have a nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

While thrombocytes lack a nuclei, they have

A

organelles and enzyme systems for generating energy and synthesizing secretory products, which are stored in granules dispersed throughout the cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Thrombocytes contain high concentrations of

A

actin and myosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Thrombocytes are disc shaped and are

A

metabolically active cytoplasmic fragments of megakaryocytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Thrombocytes (platelets) contain

A

granules in which many of the chemical mediators of hemostasis reside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Primary function of thrombocytes

A

Hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Thrombocyte count

A

150,000 - 400,000 / mm^3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where are additional thrombocytes stored?

A

Spleen!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Life span of thrombocytes

A

7-10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Thrombocytopenia

A

Platelet count of < 150,000 /mm^3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Thrombocytopenia is caused by

A

Decreased platelet production
Decreased Platelet survival
Increase Platelet consumption in spleen
Dilution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Normally, spleen reserve about 30% of platelets, an enlarged spleen will reserve

A

up to 90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does dilution contribute to thrombocytopenia

A

Overload of fluids, for example, from massive transfusions of whole blood that has been stored > 24 hours (platelets degenerate in stored blood after 24 hours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Clinical manifestation of Thrombocytopenia

A
  • Increased bruising and prolonged bleeding following minor trauma
  • Petechiae, purpura, and ecchymosis
  • Spontaneous mucosal (gingival bleeding, epistaxis [nose bleeds] ) gastrointestinal and/or intracranial bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Petechiae, Purpura and ecchymosis are

A

Leakage of blood cells into skin or mucous membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Petechiae are

A

tiny, pinpoint blotches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Purpura are

A

blotches that are larger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ecchymosis is redness that is non-blanchable (outside of vessels) and when

A

Petechiae and Purpura are combined

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Any bleeding into the skin that is > 1 cm is called

A

Ecchymosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What clinical manifestation can be seen when platelet count is 50,000 / mm^3

A

Increased bruising and prolonged bleeding following trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What clinical manifestation can be seen when platelet count is <50,000 / mm ^3

A

Petechiae, purpura, and ecchymosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What clinical manifestation can be seen when platelet count is <20,000 / mm ^3

A

Spontaneous mucosal gastrointestinal and/or intracranial bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Type of thrombocytopenia that is chronic and autoimmune

A

Immune thrombocytopenia purpura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Immune thrombocytopenia purpura is a

A

Chronic, autoimmune disorder, and is the most common cause of thrombocytopenia secondary to platelet destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does Immune thrombocytopenia purpura do to platelets?

A

Formation of antibodies against platelets cause destruction of platelets in spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Patient presentation of Immune thrombocytopenia purpura

A

History of epistaxis, bruising, petechiae, purpura, bleeding gums, Melena (blood in stool), splenomegaly (enlarged spleen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Treatment of immune thrombocytopenia purpura

A

Bleeding precautions (avoid giving injections, electric razors, etc.)
Immunosuppressants
corticosteroids (usually prednisone)
Splenectomy
Patents with platelets > 30,000/mm^3 often do not have increased mortality related to thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Thrombocythemia aka

A

Thrombocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Thrombocythemia, generally defines as

A

Platelet count > 400,000 mm^3 but usually not clinically significant until >750,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

2 types of thrombocythemia

A

Essential (primary) thrombocythemia

Secondary thrombocythemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Most common thrombocythemia

A

Essential (primary) thrombocythemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Essential (primary) thrombocythemia

A

Myeloproliferative neoplasm (cancer of bone barrow cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

essential (primary) thrombocythemia increase

A

Platelet production and often accompanied by increase of RBC production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

secondary thrombocythemia may occur after

A

Splenectomy, may be gradual, up to 3 weeks post op

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Why does secondary thrombocythemia happen after a splenectomy?

A

Short term platelet increase in system as body toys to recalibrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Reactive thrombocythemia *secondary

A

due to inflammatory conditions

cause is underlying condition like infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Clinical manifestations of thrombocythemia

A 
Increase WBC 
Leukocytosis 
Splenomegaly 
Thrombosis 
blessing 
itching 
microcirculatory symptoms, leading to ischemia in the fingers, toes, to CV regions 
Erythromyalgia 
headache 
paresthesias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Pathophysiological elevations in thrombocythemia may result in

A 
Thrombosis (DVT, Peripheral vascular ischemia) 
Thromboembolic events (pulmonary embolism)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Mechanisms of hemostasis

A

Stopping blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Endothelium

A

a type of epithelial cell that forms a single later along the inner lining of blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

The endothelium represents a

A

dynamic interface between flowing blood and the vessel wall, and produces a variety of factors that REGULATE BLOOD FLUIDITY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

he endothelium regulates the fluid state of blood through

A

its thromboresistance and profibrinolytic properties, and anti-inflammatory potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Nitric oxide

A

naturally occurring gas released from vascular endothelial cells that causes vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Prostacyclin

A
  • type of prostaglandin involved in the normal vasodilation at rest
  • anti platelet activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Endothelin

A

peptides that leas to vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How does endothelium respond to injury

A

pro clotting attributes (vWF assists in platelet adhesion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Steps of hemostasis

A
  1. Vascular spasm
  2. platelet plug formation
  3. coagulation (extrinsic and intrinsic)
  4. clot retraction
  5. fibrinolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Vascular spasm is a response when

A

there is a break in the vessel wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Hemostasis is

A

immediate and temporary response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

hemostasis is a ____ reflex

A

Neural reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

in vascular spasms, what humoral factors contribute to spasm

A

Humoral factors such as endothelia, 5-HT, and TXA2 released from platelets contribute to spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Overall, vascular spasms causes

A

Decrease in blood flow through vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Damaged vessel contains collagen, which attracts

A

platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Von Willebrand factor (vWF) is released from the endothelium which

A

binds to platelet receptors, causing platelet adhesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

When platelets are activated, they become

A
  • Enlarged and become irregularly shaped

- Form numerous spiky projections, become sticky, and expose glycoprotein receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Activated platelets expose

A

glycoprotein receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Activated platelets degranulate and release

A

ADP, 5HT, TXA2, which furthers VASOCONSTRICTION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Accumulation of large numbers of platelets cause

A

platelet aggregation which forms a mass called the platelet plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

are platelet plugs temporary or long term?

A

they are a temporary repair and is referred to as primary hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Primary hemostasis is

A

a temporary repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

clotting pathways of blood coagulation

A

Intrinsic pathway

extrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Intrinsic pathway:

A

all elements for clotting are present in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Extrinsic pathway

A

requires factor III (tissue thromboplastin) which comes from tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Intrinsic and extrinsic pathway combine to become

A

common pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Blood coagulation involves conversion of

A

fibrinogen to fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Fibrinogen is a

A

protein always present in plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Fibrin

A

Forms a meshwork that traps RBC & platelets —> clot!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

The production of fibrin is referred to as

A

secondary hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Both clotting pathways happen

A

simultaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What makes clotting permenany

A

When fibrinogen is converted to fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

The common pathway begins with

A

Prothrombin converts to thrombin, to then convert fibrinogen to fibrin
(Basically as factor 10)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What factors works on prothrombin

A

activated factor 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Most clotting factors are synthesized in

A

the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what clotting factors are synthesized in the liver

A

II, V, VII, IX, X, XI, XII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What factors are vitamin K dependent

A

Factors II (prothrombin)
VII
IX
X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

The chief sources of vitamin K are

A

Synthesis by bacteria in large intestine

Dietary (green foods)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Now that the clot is more permeate, what makes it stronger

A

clot retraction step

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Clot retraction involves

A

Consolidation and tightening of fibrin clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What pulls the edges of damaged tissue together

A

Contraction of actin and myosin in platelets pull edges of damaged tissue together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Platelets in clots…

A

bind fibrin threads together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is squeezed out in the process of clot retraction

A

serum (plasma without fibrinogen & clotting factors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

In the clot retraction process, platelets release

A

Factor XIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Factor XIII does what

A

strengthens and stabilizes the clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Clot is usually dissolved within a few days after clot formation by

A

fibrinolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What happens in fibrinolysis

A

Slow release of tissue plasminogen activator (t-PA) from injured tissue converts plasminogen to plasmin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Plasmin (enzyme) causes

A

Dissolution of the clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Plasmin chops through fibrin and

A

digests fibrin threads and inactivates clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Disorders of coagulation

A 
Vitamin K deficiency 
Liver disease 
Venous thromboembolism 
Pulmonary embolism 
Von Willebrand disease 
Hemophilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Vitamin K is a

A

Fat-soluble vitamin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

where is vitamin K stored

A

in the liver and fat tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Vitamin KK is necessary for the

A

synthesis and regulation of prothrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Most common sources of Vitamin K is

A

green leafy vegetables

96
Q

Primary reason for vitamin K deficiency is

A

Total parenteral nutrition (TPN) with antibiotics that destroy the GI flora

97
Q

Liver disease may include

A

Hepatocellular disease, cirrhosis, etc.

98
Q

What site is where most of clotting factors are produced

A

Liver

99
Q

Damage to the liver cells leads to

A

significant decrease in most clotting factors (Factor VII)

diminished levels are clotting system regulators (antithrmbin)

100
Q

Challenging clinical manifestions in liver disease

A

Thrombocytopenia

Pooling of platelets in the spleen, often leading to portal hypertension

101
Q

Thrombosis is

A

hemostasis in the wrong place

102
Q

A thrombus is a

A

stationary blood clot in the cardiovascular system (VENOUS OR ARTERIAL)

103
Q

Predisposing factors for thrombus formation

A

Stasis
Hypercoagulability
Endothelial damage (vessel wall/abnormality)

104
Q

Two manifestations of venous thromboembolism (VTE)

A

Deep VEIN thrombosis

Acute pulmonary

105
Q

2 categories of deep vein thrombosis

A

Distal (calf) vein thrombosis, in which thrombi remain confined to the deep calf veins
Proximal veins thrombosis, in which thrombosis involves the popliteal, femoral, or iliac veins

106
Q

Which is clinically of great importance, distal or proximal vein thrombosis

A

Proximal vein is of greater importance clinically, since it is more commonly associated with the development of PE

107
Q

What can happen from a proximal vein thrombosis

A

Can follow venous flow into right side of the heart and get longed in the pulmonary vasculature and cause acute pulmonary embolism

108
Q

Risk factors for venous thromboembolism

A 
Recent surgery 
History of immobilization (long haul travel) or prolonged hospitalization/bed rest 
obesity 
Prior episode of venous thromboembolism 
lover extremity trauma 
malignancy 
oral contraceptives 
pregnancy or postpartum 
peripheral vascular disease 
diabetics 
lung disease or who smoke
109
Q

Pulmonary embolism

A

Life threatening complication of venous thromboembolism

110
Q

Thrombus becomes an embolus when it is

A

no longer stationary

111
Q

Embolus tend to travel

A

towards heard

Cardiac circulation –> pulmonary artery –> lungs

112
Q

Large percentage of pulmonary embolisms (PE) are

A

clinically silent

113
Q

Pulmonary infarction occurs in up to

A

20%

114
Q

Pulmonary embolism is fatal in

A

1% patents

115
Q

DVT is associated with >600,000 US hospitals annually and result in

A

> 200,000 death from pulmonary embolism

116
Q

Von willebrand disease

A

An inherited blood-clotting disorder

117
Q

Von villebrand disease is an

A

autosomal dominant, three type, 20 variants

118
Q

one of three types of von-willebrand disease is

A

Autosomal recessive, vWD type 3

119
Q

The most common type of vWD

A

type I

120
Q

vWD is characterized by

A

Von willebrand factor

121
Q

Von willebrand factor is a

A

plasma protein

122
Q

What does von willebrand factor so

A

helps platelets stick to injured blood vessels during formation of blood clots (builds a bridge activated platelet & endothelium from platelets)

123
Q

vWF also is a carrier and stabilizer for

A

Factor VIII

124
Q

deficiency of vWf also means

A

deficiency inhibits multilevel clotting factors

125
Q

Patient presentation of von willebrand disease

A

Evidence of mild ecchymosis (discoloration under skin)

Bleeding (nose, gums, GI, menorrhagia) with NORMAL platelet count

126
Q

treatment of von willebrand disease

A

Bleeding precautions
avoidance of aspirin
DDAVP (vasopressin) which stimulates release of stored vWF from endothelial cells
—-LEADING TO VASOCONSTRICTION + FLUID RETENTION

127
Q

Most classic hemophilia

A

Hemophilia A “classic hemophilia”

128
Q

Hemophilia is a

A

X-linked disorder (or may arise from a new mutation of the F8 gene)

129
Q

Hemophilia A is caused by

A

mutation on the F8 gene that provides instructions to make factor VIII

130
Q

Hemophilia causes a

A

lack of VIII factor

131
Q

A lack of factor VIII causes

A 
spontaneous bleeding into soft tissues, GI tract, Hip, Knee, elbow, ankles 
inflammation 
pain 
swelling 
bruising 
deformities 
immobilization 
bleeding into brain from brain injury
132
Q

hemophilia mutant gene is on

A

X chromosome

133
Q

Most affected persons of hemophilia are

A

male, affected females are extremely rare

134
Q

As a X-linked inheritance

A

all affected males never transmit gene to sons

all daughters of an male are carriers, none are affected

135
Q

Sons of carrier females have

A

50 % chance of inheriting it and being infected

136
Q

Daughters of carrier females have

A

50% of inheriting and carrying

137
Q

managements of hemophilia

A

infusions of factor VIII (human or recombinant)

138
Q

for mild disease of hemophilia: management

A

Desmopressin acetate (DDAVP)

139
Q

Desmopressin acetate (DDAVP) stimulates

A

release of vWF from endothelium which increases factor VIII levels 2-3 fold
VASOCONSTRICTION)

140
Q

hemophilia pateitns should

A

Avoid contact sports

bleeding precautions

141
Q

aPTT

A

Activated partial thromboplastin time

142
Q

aPTT evaluates the

A

intrinsic and final common pathways

143
Q

aPTT is the

A

length of time for blood to clot

144
Q

Normal value for aPTT

A

30-40 seconds

145
Q

What medication increases aPTT

A

Heperain

146
Q

Those on heparin, aPTT labs should be

A

1.5 0 2.5 times the normal range is considered therapeutic level

147
Q

With heparin, we are looking for

A

prolonged aPTT because we want decrease risk of clotting

148
Q

PT

A

Prothrombin time

149
Q

PT evaluates the

A

extrinsic and final common pathway

150
Q

PT is

A

the length of time for the blood to clot

151
Q

Normal time for PT

A

10-14 seconds

152
Q

Those on warfarin, PT labs would be

A

1.5-2.5 times the normal range to be considered therapeutic

153
Q

INR

A

International normalized ratio

154
Q

When patent that takes medication that acts on extrinsic factor, check

A

PT and INR

155
Q

INR evaluates

A

extrinsic pathway, but provides uniformity worldwide (independent of reagents)

156
Q

INR is most often used to monitor patent on

A

warfarin

157
Q

1.5 INR

A

low level anticoagulation (Prophylaxis)

158
Q

2.0-3.0 INR

A

Medium level anticoagulation (DV, stroke, PE, prophylaxis, MI)

159
Q

2.5 - 3.5 INR

A

High level anticoagulation (DVT, mechanical heart valve)

160
Q

High alert medications =

A

Medications that have the highest risk of causing injury when miused

161
Q

Top 5 high alert medications

A 
Insulin 
Opiates 
Injectable potassium chloride 
Anticoagulants 
Sodium chloride solutions above .9%
162
Q

Safety goal for anticoagulant medications

A

reduce the likelihood of patient harm associated with the use of anticoagulation therapy

163
Q

anticoagulation therapy is used for a number of conditions, including

A

Atrial fibrillation
Deep vein thrombosis
Pulmonary embolism
Heart valve replacement

164
Q

Anticoagulant medications are more likely than other medications to cause harm due to

A

complex dosing, insufficient monitoring, & inconsistent patient adherence

165
Q

Healthcare organizations that provide anticoagulant therapy MUST have

A

a process in place to reduce the risk of anti-coagulant associated patient harm

166
Q

types of coagulation modifiers

A

Anticoagulants
Antiplatelet agents
Thrombolytics

167
Q

Overall, anticoagulants

A

prevent coagulation and clot formation

168
Q

Overall, anti platelet agents

A

act on platelets

169
Q

overall, thrombolytics

A

lyse clots

170
Q

Anticoagulants are drugs that

A

prevent the formation of a clot by inhibiting certain clotting factors

171
Q

Three main types of anticoagulants

A

Heparins
Vitamin K antagonists
Direct Thrombin inhibitors

172
Q

Indications for anticoagulants

A

High risk of clot formation (MI, Unstable angina, AF, uses of indwelling devices (heart valves)
Major orthopedic surgeries
prolonged immobilization

173
Q

Anticoagulants are also used in the treatment of

A

Ischemic complications of unstable angina, some dysrthymias, and disseminated intravascular coagulation

174
Q

Heparin targets which pathway

A

Intrinsic pathway

175
Q

Heparin mOA

A

Combine with antithrombin III (natural anticoagulant) to inactive clotting factors 9,10,11,12
which inhibit the conversion of prothrombin to thrombin

176
Q

after thrombosis, heparin can also

A

inactivate thrombin, preventing the conversion of fibrinogen to fibrin

177
Q

Adverse effects of heparin

A

Hemorrhage
Neurologic damage
Thrombocytopenia (heparin-induced thrombocytopenia)
Hypersensitivity reactions

178
Q

Heparin half life

A

super short

179
Q

Nursing considerations and adverse effects of heparin

A

Local irritation and hematoma from SQ injections
Hemmorage
Monitor for heparin induced thrombocytopenia
Monitor for hypersensitivity reactions (animal antigens): manifested by chills, fever, urticaria, anaphylaxis

180
Q

antidote for heparin

A

Protamine sulfate

181
Q

Protamine sulfate MoA

A

Binds with heparin to form a stable complex that can be eliminated

182
Q

Signs of bleeding

A 
Bruises
Petechiae
Red or black stools
Discolored urine
Pelvic pain
Lumbar pain
Headache
183
Q

Black box warning for heparin

A

some heparin products contain benzyl alcohol (preservative)
Contraindicated in neonates (Fatal toxicity!)
USE PRESERVATIVE FREE HEPARIN

184
Q

Enoxaparin drug class

A

Low molecular weight heparin (LMWH), anticoagulant

185
Q

Enoxaparin is basically heparin that is

A

composed of shorter molecules that unfractionated heparin

186
Q

Enoxaparin indications

A

Same as heparin
Prophylaxis/treatment of thromboembolism (especially with orthopedic surgery/bariatric surgery)
Adjunct to percutaneous coronary intervention
Unstable angina
acute coronary syndrome

187
Q

MoA enoxaparin

A

Potentiates the effect of antithrombin III, making it a rapid INACTIVATOR of coagulation factor Xa, which inhibits factor Xa, inhibiting thrombin, thus the anticoagulant effect

188
Q

Enoxaparin effects which pathway

A

Intrinsic pathway

189
Q

Antidote for enoxaparin

A

protamine sulfate

190
Q

Half life of enoxaparin

A

extended, so the dose is less often

191
Q

Adverse effects of enoxaparin

A

similar side effects of heparin, bleeding less frequent

192
Q

Protamine sulfate nursing considerations

A

Rapid administration can cause severe HYPOtension & anaphylactoid reactions (max 50 mg over 10 min)
Monitor vital signs closey during administration, monitor aPTT

193
Q

Black box warning protamine sulfate

A
  • Severe hypersensitivity reactions (hypotension, cardiovascular collapse, pulmonary hypertension, pulmonary edema)
  • Risk increased with high doses, repeated doses, previous protamine administration
194
Q

Warfarin drug class

A

Vitamin K Antagonist, anticoagulant

195
Q

Warfarin effects which pathway

A

Extrinsic + Common pathway

196
Q

Warfarin MoA

A

Acts int he liver to prevent synthesis of vitamin K dependent clotting factors (2,7,9,10)

197
Q

Adverse effects of warfarin

A 
Hemorrhage 
Nausea/vomitting 
Abdominal pain 
Alopecia 
Uticaria 
Dizziness 
Joint or muscle pain
198
Q

Warfarin Nursing considerations

A

Monitor PT, INR (2-3 range), baseline, then at intervals

199
Q

2nd most common drug

A

warfarin

200
Q

Warfarin patient teaching

A
  • Avoid situations that may result in injury, bleeding precautions (electric razors)
  • Monitor for bleeding (gingival bleeding, tarry stool, bloody sputum, hematuria, internal bleeding
  • INR monitoring
  • wear medic identifications
  • Dietary considerations
201
Q

When taking warfarin, patients should do what with their diet

A

Keep diet CONSISTENT with foods that are high in vitamin K (avocado, broccoli, lettuce, egg yolk)
— Increasing vitamin can decrease effectiveness of warfarin

202
Q

OTC and warfarin patent teaching

A

Avoid taking over-the-counter NSAIDS, especially aspiring or drugs containing salicylates
— basically avoid drugs that target COX 1

203
Q

Antidote for warfarin

A

VITAMIN K

204
Q

Heparin onset

A

RAPID (minutes)

205
Q

Warfarin onset

A

SLOW (hours)

206
Q

Dabigatran drug class

A

Direct Thrombin Inhibitors, anticoagulants

207
Q

Dabigatran moA

A

direct and reversible inhibition of thrombin

208
Q

Direct Thrombin Inhibitors have no known

A

antagonists

209
Q

Dabigatran effects which pathway

A

Common pathway

210
Q

Dabigatran indications

A

anticoagulation to prevent strokes
systemic embolization in individuals with nonvalvular atrial fibrillation
– treatment and prevention of deep vein thrombosis and pulmonary embolism

211
Q

Dabigatran adverse effects

A 
Bleeding 
Nausea
Vomitting 
anemia
Hematoma 
Elevated liver function tests
212
Q

4 types of anti platelet drugs

A

Salicylates
Adenosine diphosphate receptor (ADP) inhibitors
Glycoprotein inhibitors
Arterial vasodilators

213
Q

Aspirin drug class

A

Antiplatelet drugs, salicylates

214
Q

Aspirin indications

A

inhibit platelet aggregation

Reduce risk for: MI, Ischemic cerebrovascular accident, angina

215
Q

aspring prevents reocclusion of

A

Coronary stents

216
Q

Clopidogrel drug class

A

Adenosine diphosphate (ADP) receptor antagonist

217
Q

Clopidogrel indications

A
  • Prevent stenosis of coronary stents
  • Decrease risk of death due to thrombotic events (MI, stroke, embolism) in patients w/ atherosclerosis
  • Peripheral arterial disease history of MI and stroke

—– Decreases ADP aggregation which decreases platelet aggregation

218
Q

Clopidogrel moA

A

IRREVERSIBLE blockade of ADP receptors on platelet surface, which prevents ADP-stimulated aggregation

219
Q

Clopidogrel requires

A

biotransformation into active metabolite

220
Q

Clopidogrel administration

A

PO only

221
Q

Clopidogrel adverse effects

A 
bleeding 
dyspepsia 
diarrhea 
rash 
chest pain 
purpura 
atrial arrhythmias 
edema 
GI hemorrhage
222
Q

Clopidogrel nursing consideration

A

Monitor signs and symptoms of bleeding
Monitor Hemoglobin & hematocrit, platelets at baseline and periodically
Contraindicated in active blessing
Concurring use with NSAIDS, aspirin, and other anticoagulants may increase bleeding

223
Q

When should clopidogrel be discontinued

A

discontinue 5-10 days before invasive procedures (as with any antiplatelet/anticoagulant)

224
Q

What group of patients are poor metabolizers of clopidogrel

A

Patients with one or more copies of the variant CYP2C192 &/or CYP2C193

225
Q

Patients with one or more copies of the variant CYP2C192 &/or CYP2C193 may have

A

lower reduced conversion of clopidogrel to its active metabolite
Lower active metabolite exposure may result in reduce platelet inhibition

226
Q

abciximab drug class

A

Glycoprotein inhibitor, anti platelet

227
Q

Abciximab indications

A

Patients undergoing coronary artery procedures such as angioplasty

228
Q

Abciximab moA

A

Prevents platelets from sticking together (adhesion) and causing thrombus (blood clot) formation within the coronary artery
– targets platelet adhesion, decrease sticky ability

229
Q

Thrombolytics are used when

A

clot has been formed, and needs to be dissolved

230
Q

Thrombolytics are coagulation modifiers that

A

lyse thrombi in the blood vessels to establish blood flow

231
Q

Atleplase drug class

A

Thrombolytics

232
Q

Alteplase administration

A

IV

233
Q

Alteplase moA

A

a naturally occurring tissue plasminogen activator (t-PA) produced through recombinant DNA techniques

234
Q

Alteplase indications

A 
Acute MI 
Arterial thrombosis 
DVT 
Occlusion of shunts or catheters 
Pulmonary embolism 
Acute thrombotic stroke
235
Q

Alteplase adverse effects

A

Internal, intracranial, and superficial bleeding

precipitate cardiac dysrhythmias

316 Pharmacology (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions